**Core Concept**
The pathogenesis of duodenal ulcers involves an imbalance between mucosal defense and acid-pepsin secretion, with Helicobacter pylori infection and nonsteroidal anti-inflammatory drugs (NSAIDs) being major contributing factors.

**Why the Correct Answer is Right**
Helicobacter pylori infection is a well-established cause of duodenal ulcers, leading to chronic gastritis and mucosal damage. The bacterium's urease enzyme breaks down gastric mucus, reducing its protective effect and allowing acid-pepsin to come into contact with the mucosa. This results in mucosal damage and ulcer formation. Additionally, H. pylori infection can lead to increased acid production and reduced mucosal blood flow, further contributing to ulcer development.

**Why Each Wrong Option is Incorrect**
* **Option A:** Although stress is a contributing factor, it is not a causative agent for duodenal ulcers. Stress can exacerbate existing ulcers by increasing acid production and reducing mucosal blood flow.
* **Option B:** Smoking is a risk factor for duodenal ulcers, but it is not a direct causative agent. Smoking can reduce mucosal blood flow and increase acid production, but these effects are secondary to the primary cause.
* **Option C:** While NSAIDs can cause duodenal ulcers by reducing mucosal prostaglandins and increasing acid production, they are not a causative agent in the same way as H. pylori infection.

**Clinical Pearl / High-Yield Fact**
Remember that H. pylori infection is a major cause of duodenal ulcers, and treatment should involve eradication of the bacterium in addition to acid-reducing medications.

**Correct Answer:** C. H. pylori